The blood pressure lowering effect of aminoglutethimide (AG) (1 gm/day for 2 week) was compared with its effect on the major pathways of adrenal steroid biosynthesis in 4 patients with LREH and in 2 patients with normal renin essential hypertension (NREH). AG reduced BP in all patients, and decreased the excretion of aldosterone 75 per cent, but failed to decrease plasma concentrations of progesterone, 17-hydroxyprogesterone, deoxycorticosterone, 11-desoxycortisol, or cortisol, or the urinary excretion of 16-beta-OH-dehydroepiandrosterone, 17-hydroxy or 17-ketosteroids. Secretion rates for 16-beta-OH DHEA were not changed by AG. BP-lowering action of AG in LREH probably resulted from inhibition of aldosterone synthesis; 16-beta-OH-DHEA is unimportant in LREH because its secretion is not reduced when BP is lowered by AG; Na ion-retaining steroids other than aldosteron are not important in LREH because no other major steroid pathway was inhibited by AG; AG altered steroid synthesis similarly in 2 normal-renin hypertensive patients but lowered BP less, possibly because their plasma renin during AG was 5 times greater than that of LREH patients.